Oral retinoids are a type of medicine used to treat severe acne. They’re sold under the brand name Roaccutane, among others.

While oral retinoids are very effective, they can have harmful effects if taken during pregnancy. These medicines can cause miscarriages and major congenital abnormalities (harm to unborn babies) including in the brain, heart and face. At least 30% of children exposed to oral retinoids in pregnancy have severe congenital abnormalities.

Neurodevelopmental problems (in learning, reading, social skills, memory and attention) are also common.

Because of these risks, the Australasian College of Dermatologists advises oral retinoids should not be prescribed a month before or during pregnancy under any circumstances. Dermatologists are instructed to make sure a woman isn’t pregnant before starting this treatment, and discuss the risks with women of childbearing age.

But despite this, and warnings on the medicines’ packaging, pregnancies exposed to oral retinoids continue to be reported in Australia and around the world.

In a study published this month, we wanted to find out what proportion of Australian women of reproductive age were taking oral retinoids, and how many of these women were using contraception.

Our results suggest a high proportion of women are not using effective contraception while on these drugs, indicating Australia needs a strategy to reduce the risk oral retinoids pose to unborn babies.

Contraception options

Using birth control to avoid pregnancy during oral retinoid treatment is essential for women who are sexually active. Some contraception methods, however, are more reliable than others.

Long-acting-reversible contraceptives include intrauterine devices (IUDs) inserted into the womb (such as Mirena, Kyleena, or copper devices) and implants under the skin (such as Implanon). These “set and forget” methods are more than 99% effective.

The effectiveness of oral contraceptive pills among “perfect” users (following the directions, with no missed or late pills) is similarly more than 99%. But in typical users, this can fall as low as 91%.

Condoms, when used as the sole method of contraception, have higher failure rates. Their effectiveness can be as low as 82% in typical users.

Oral retinoid use over time

For our study, we analysed medicine dispensing data among women aged 15–44 from Australia’s Pharmaceutical Benefit Scheme (PBS) between 2013 and 2021.

We found the dispensing rate for oral retinoids doubled from one in every 71 women in 2013, to one in every 36 in 2021. The increase occurred across all ages but was most notable in young women.

Most women were not dispensed contraception at the same time they were using the oral retinoids. To be sure we weren’t missing any contraception that was supplied before the oral retinoids, we looked back in the data. For example, for an IUD that lasts five years, we looked back five years before the oral retinoid prescription.

Our analysis showed only one in four women provided oral retinoids were dispensed contraception simultaneously. This was even lower for 15- to 19-year-olds, where only about one in eight women who filled a prescription for oral retinoids were dispensed contraception.

A recent study found 43% of Australian year 10 and 69% of year 12 students are sexually active, so we can’t assume this younger age group largely had no need for contraception.

One limitation of our study is that it may underestimate contraception coverage, because not all contraceptive options are listed on the PBS. Those options not listed include male and female sterilisation, contraceptive rings, condoms, copper IUDs, and certain oral contraceptive pills.

But even if we presume some of the women in our study were using forms of contraception not listed on the PBS, we’re still left with a significant portion without evidence of contraception.

What are the solutions?

Other countries such as the United States and countries in Europe have pregnancy prevention programs for women taking oral retinoids. These programs include contraception requirements, risk acknowledgement forms and regular pregnancy tests. Despite these programs, unintended pregnancies among women using oral retinoids still occur in these countries.

But Australia has no official strategy for preventing pregnancies exposed to oral retinoids. Currently oral retinoids are prescribed by dermatologists, and most contraception is prescribed by GPs. Women therefore need to see two different doctors, which adds costs and burden.

Rather than a single fix, there are likely to be multiple solutions to this problem. Some dermatologists may not feel confident discussing sex or contraception with patients, so educating dermatologists about contraception is important. Education for women is equally important.

A clinical pathway is needed for reproductive-aged women to obtain both oral retinoids and effective contraception. Options may include GPs prescribing both medications, or dermatologists only prescribing oral retinoids when there’s a contraception plan already in place.

Some women may initially not be sexually active, but change their sexual behaviour while taking oral retinoids, so constant reminders and education are likely to be required.

Further, contraception access needs to be improved in Australia. Teenagers and young women in particular face barriers to accessing contraception, including costs, stigma and lack of knowledge.

Many doctors and women are doing the right thing. But every woman should have an effective contraception plan in place well before starting oral retinoids. Only if this happens can we reduce unintended pregnancies among women taking these medicines, and thereby reduce the risk of harm to unborn babies.

Dr Laura Gerhardy from NSW Health contributed to this article.

Antonia Shand, Research Fellow, Obstetrician, University of Sydney and Natasha Nassar, Professor of Paediatric and Perinatal Epidemiology and Chair in Translational Childhood Medicine, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

A recent study has suggested Shingrix, a relatively new vaccine given to protect older adults against shingles, may delay the onset of dementia.

This might seem like a bizarre link, but actually, research has previously shown an older version of the shingles vaccine, Zostavax, reduced the risk of dementia.

In this new study, published last week in the journal Nature Medicine, researchers from the United Kingdom found Shingrix delayed dementia onset by 17% compared with Zostavax.

So how did the researchers work this out, and how could a shingles vaccine affect dementia risk?

From Zostavax to Shingrix

Shingles is a viral infection caused by the varicella-zoster virus. It causes painful rashes, and affects older people in particular.

Previously, Zostavax was used to vaccinate against shingles. It was administered as a single shot and provided good protection for about five years.

Shingrix has been developed based on a newer vaccine technology, and is thought to offer stronger and longer-lasting protection. Given in two doses, it’s now the preferred option for shingles vaccination in Australia and elsewhere.

In November 2023, Shingrix replaced Zostavax on the National Immunisation Program, making it available for free to those at highest risk of complications from shingles. This includes all adults aged 65 and over, First Nations people aged 50 and older, and younger adults with certain medical conditions that affect their immune systems.

What the study found

Shingrix was approved by the US Food and Drugs Administration in October 2017. The researchers in the new study used the transition from Zostavax to Shingrix in the United States as an opportunity for research.

They selected 103,837 people who received Zostavax (between October 2014 and September 2017) and compared them with 103,837 people who received Shingrix (between November 2017 and October 2020).

By analysing data from electronic health records, they found people who received Shingrix had a 17% increase in “diagnosis-free time” during the follow-up period (up to six years after vaccination) compared with those who received Zostavax. This was equivalent to an average of 164 extra days without a dementia diagnosis.

The researchers also compared the shingles vaccines to other vaccines: influenza, and a combined vaccine for tetanus, diphtheria and pertussis. Shingrix and Zostavax performed around 14–27% better in lowering the risk of a dementia diagnosis, with Shingrix associated with a greater improvement.

The benefits of Shingrix in terms of dementia risk were significant for both sexes, but more pronounced for women. This is not entirely surprising, because we know women have a higher risk of developing dementia due to interplay of biological factors. These include being more sensitive to certain genetic mutations associated with dementia and hormonal differences.

Why the link?

The idea that vaccination against viral infection can lower the risk of dementia has been around for more than two decades. Associations have been observed between vaccines, such as those for diphtheria, tetanus, polio and influenza, and subsequent dementia risk.

Research has shown Zostavax vaccination can reduce the risk of developing dementia by 20% compared with people who are unvaccinated.

But it may not be that the vaccines themselves protect against dementia. Rather, it may be the resulting lack of viral infection creating this effect. Research indicates bacterial infections in the gut, as well as viral infections, are associated with a higher risk of dementia.

Notably, untreated infections with herpes simplex (herpes) virus – closely related to the varicella-zoster virus that causes shingles – can significantly increase the risk of developing dementia. Research has also shown shingles increases the risk of a later dementia diagnosis.

The mechanism is not entirely clear. But there are two potential pathways which may help us understand why infections could increase the risk of dementia.

First, certain molecules are produced when a baby is developing in the womb to help with the body’s development. These molecules have the potential to cause inflammation and accelerate ageing, so the production of these molecules is silenced around birth. However, viral infections such as shingles can reactivate the production of these molecules in adult life which could hypothetically lead to dementia.

Second, in Alzheimer’s disease, a specific protein called Amyloid-β go rogue and kill brain cells. Certain proteins produced by viruses such as COVID and bad gut bacteria have the potential to support Amyloid-β in its toxic form. In laboratory conditions, these proteins have been shown to accelerate the onset of dementia.

What does this all mean?

With an ageing population, the burden of dementia is only likely to become greater in the years to come. There’s a lot more we have to learn about the causes of the disease and what we can potentially do to prevent and treat it.

This new study has some limitations. For example, time without a diagnosis doesn’t necessarily mean time without disease. Some people may have underlying disease with delayed diagnosis.

This research indicates Shingrix could have a silent benefit, but it’s too early to suggest we can use antiviral vaccines to prevent dementia.

Overall, we need more research exploring in greater detail how infections are linked with dementia. This will help us understand the root causes of dementia and design potential therapies.

Ibrahim Javed, Enterprise and NHMRC Emerging Leadership Fellow, UniSA Clinical & Health Sciences, University of South Australia

This article is republished from The Conversation under a Creative Commons license. Read the original article.